Recently an intravenous injection of a virus vector encoding human Factor IX, which is deficient in Hemophilia B was shown to increase Factor IX concentration in the serum of subjects with Hemophilia B to a degree that lowered their requirements for exogenous Factor IX infusion. However: 1) this protein was not under regulated expression, and therefore, did not enable optimal tailoring of levels of the transgene in the serum, 2) this system did not provide for a means to turn off transgene expression in case of undesired or unexpected effects, and 3) the gene, Factor IX, was not a paracrine gene, and had no beneficial cardiovascular effects, and therefore, could not be used to treat heart disease.